Chapter 16 Structure and functional anatomy of visceroreceptors in the mammalian respiratory system

M, von Düring; Kh, Andres

doi:10.1016/s0079-6123(08)63008-3

Cited by 14 publications

(5 citation statements)

References 30 publications

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“…Vagal sensory fibers innervate the majority of the viscera with free nerve terminals. Electron microscopy of these 1–2 micro-thick fiber terminals are densely packed with mitochondria, but lack overt ER-like structures (Hung et al, 1973; Kikuchi, 1976; Neuhuber, 1987; von During and Andres, 1988). Despite these reports, we found evidence of a functional ER at vagal nerve growth cone/neurites.…”

Section: Discussionmentioning

confidence: 99%

Store-operated calcium entry in vagal sensory nerves is independent of Orai channels

et al. 2013

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Vagal sensory nerves innervate the majority of visceral organs (e.g. heart, lungs, GI tract, etc) and their activation is critical for defensive and regulatory reflexes. Intracellular Ca2+ is a key regulator of neuronal excitability and is largely controlled by the Ca2+ stores of the endoplasmic reticulum. In other cell types store-operated channels (SOC) have been shown to contribute to the homeostatic control of intracellular Ca2+. Here, using Ca2+ imaging, we have shown that ER depletion in vagal sensory neurons (using thapsigargin or caffeine) in the absence of extracellular Ca2+ evoked Ca2+ influx upon reintroduction of Ca2+ into the extracellular buffer. This store-operated Ca2+ entry (SOCE) was observed in approximately 25–40% of vagal neurons, equally distributed among nociceptive and non-nociceptive sensory subtypes. SOCE was blocked by Gd3+ but not by the Orai channel blocker SKF96365. We found Orai channel mRNA in extracts from whole vagal ganglia, but when using single cell RT-PCR analysis we found only 3 out of 34 neurons expressed Orai channel mRNA, indicating that Orai channel expression in the vagal ganglia was likely derived from non-neuronal cell types. Confocal microscopy of vagal neurons in 3 day cultures demonstrated rich ER tracker fluorescence throughout axonal and neurite structures and ER store depletion (thapsigargin) evoked Ca2+ transients from these structures. However, no SOCE could be detected in the axonal/neurite structures of vagal neurons. We conclude that SOCE occurs in vagal sensory neuronal cell bodies through non-Orai mechanisms but is absent at nerve terminals.

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Section: Discussionmentioning

confidence: 99%

Store-operated calcium entry in vagal sensory nerves is independent of Orai channels

et al. 2013

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“…However it is becoming increasingly clear that mitochondrial ROS play critical roles in physiological signaling downstream of multiple pathways [123], including hypoxia [124, 125], TNFα [126], neurotrophins via p75NTR [127], Toll-like Receptors [128, 129] and TGFβ [130]. Importantly, afferent terminals innervating the peripheral tissue, including the airways, are densely packed with mitochondria [131–133]. Thus both mitochondria and afferent receptors are co-localized.…”

Section: Sources Of Neuronal Rosmentioning

confidence: 99%

Role of reactive oxygen species and TRP channels in the cough reflex

Taylor‐Clark

2016

Cell Calcium

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The cough reflex is evoked by noxious stimuli in the airways. Although this reflex is essential for health, it can be triggered chronically in inflammatory and infectious airway disease. Neuronal transient receptor potential (TRP) channels such as ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) are polymodal receptors expressed on airway nociceptive afferent nerves. Reactive oxygen species (ROS) and other reactive compounds are associated with inflammation, from either NADPH oxidase or mitochondria. These reactive compounds cause activation and hyperexcitability of nociceptive afferents innervating the airways, and evidence suggests key contributions of TRPA1 and TRPV1.

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“…The peripheral nerve terminals of vagal airway sensory fibers are densely packed with mitochondria [51–53]. Mitochondria can also be observed in axonal terminals of vagal neurons in long-term culture [54].…”

Section: Afferent Terminal Mitochondria As a Potential Source Of Rosmentioning

confidence: 99%

Oxidative stress as activators of sensory nerves for cough

Taylor‐Clark

2015

Pulmonary Pharmacology & Therapeutics

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Excessive activation of the cough reflex is a major clinical problem in respiratory diseases. The cough reflex is triggered by activation of nociceptive sensory nerve terminals innervating the airways by noxious stimuli. Oxidative stress is a noxious stimuli associated with inhalation of pollutants and inflammatory airway disease. Here, we discuss recent findings that oxidative stress, in particular downstream of mitochondrial dysfunction, evokes increased electrical activity in airway nociceptive sensory nerves. Mechanisms include activation of transient receptor potential (TRP) channels and protein kinase C. Such mechanisms may contribute to excessive cough reflexes in respiratory diseases.

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Chapter 16 Structure and functional anatomy of visceroreceptors in the mammalian respiratory system

Cited by 14 publications

References 30 publications

Store-operated calcium entry in vagal sensory nerves is independent of Orai channels

Store-operated calcium entry in vagal sensory nerves is independent of Orai channels

Role of reactive oxygen species and TRP channels in the cough reflex

Oxidative stress as activators of sensory nerves for cough

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